Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Kidney Int. 2023 Oct;104(4):646-649. doi: 10.1016/j.kint.2023.07.011.
Previous studies have indicated that succinate accumulation during kidney ischemia, and its oxidation during reperfusion, results in the production of excessive reactive oxygen species, mitochondrial dysfunction, and kidney injury. In this issue, Oh et al. have reported that pyruvate dehydrogenase kinase 4 (PDK4) inhibition in proximal tubules ameliorates kidney ischemia/reperfusion injury via suppressed succinate accumulation. This study suggests that PDK4 inhibition is a promising new treatment strategy for ischemic acute kidney injury.
先前的研究表明，肾脏缺血时琥珀酸的积累，以及再灌注时的氧化，导致了过量的活性氧物质的产生、线粒体功能障碍和肾脏损伤。在本期杂志中，Oh 等人报道了近端肾小管中丙酮酸脱氢酶激酶 4（PDK4）的抑制可通过抑制琥珀酸的积累来改善肾缺血/再灌注损伤。这项研究表明，PDK4 抑制可能是一种治疗缺血性急性肾损伤的有前途的新策略。
